衰老与组织微环境的刻板变化有关，这些变化增加了老年人对疾病的易感性，包括器官纤维化和癌症。从组织的角度来看，纤维化和癌症都可以被视为不愈合的伤口，基质中组织修复途径的致病性激活。如果纤维化和癌症代表了不同病理中适应不良基质反应趋同进化的一个例子，那么在这两种疾病中可能出现哪些在身份和功能上具有相似性的类似细胞类型？在这篇综述中，我们探讨了衰老的成纤维细胞如何形成将衰老器官与纤维化和癌症联系起来的纽带。单细胞测序的出现，加上对体内具有衰老特征的细胞类型的改进检测，使我们能够识别在纤维化和癌症中具有相似特性的衰老成纤维细胞，这些细胞具有促纤维化程序。除了在疾病状态下重组细胞外基质的能力外，这些促纤维化的衰老成纤维细胞还可以促进上皮重编程和免疫重新布线，从而推动纤维化和癌症的疾病进展。最后，纤维化和癌症中常见致病细胞类型的鉴定也为通过共同方法针对这两种疾病提供了治疗机会。版权所有 © 2024。由 Elsevier Ltd 出版。

Aging is associated with stereotyped changes in the tissue microenvironment that increase susceptibility to diseases of the elderly, including organ fibrosis and cancer. From a tissue perspective, fibrosis and cancer can both be viewed as non-healing wounds with pathogenic activation of tissue repair pathways in the stroma. If fibrosis and cancer represent an example of the convergent evolution of maladaptive stromal responses in distinct pathologies, what are the analogous cell types that might emerge in both diseases that share similarities in identity and function? In this review, we explore how senescent fibroblasts form a nexus that connects the aging organ with both fibrosis and cancer. The advent of single cell sequencing, coupled with improved detection of cell types with senescent traits in vivo, have allowed us to identify senescent fibroblasts with similar identities in both fibrosis and cancer that share pro-fibrotic programs. In addition to their ability to reorganize the extracellular matrix in diseased states, these pro-fibrotic senescent fibroblasts can also promote epithelial reprogramming and immune rewiring, which drive disease progression in fibrosis and cancer. Finally, the identification of common pathogenic cell types in fibrosis and cancer also presents a therapeutic opportunity to target both diseases with a shared approach.Copyright © 2024. Published by Elsevier Ltd.